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PubMed1977

[Factors in the progression and propagation of arteriosclerosis. Results of an interdisciplinary study (author's transl)].

Starting from generalized theories of the arteriosclerosis, a comprehensive model of factor analysis is presented which considers the clinical risk spectrum of coronary heart disease as presently known. Arteriosclerosis and morphological findings are also included in the analysis. A differentiation is made between "progressive remification" and "multiple variable" patterns, which combine the clinical risks in a specific structure. Fractions of unknown influencing factors could be estimated quantitatively and qualitatively in such a manner that suggestions concerning the huge dependency of time and the progressive increase with age could be determined.

Adult↗

PubMed1982

Effects of unilateral nephrectomy on erythrocytosis and arteriosclerosis induced in rats by intrarenal injection of nickel subsulfide.

Administration of Ni3S2 to rats by unilateral inrarenal (ir) injection (5 mg/rat) caused erythrocytosis, arteriosclerosis, and abnormal plasma concentrations of asparagine, glycine, histidine, and lysine. Resection of the ipsilateral (Ni3S2-treated) kidney on the fourth day after the ir injection prevented erythrocytosis, amino acid disturbances, and severe arteriosclerotic lesions (fibrous intimal plaques and focal medial necrosis), but did not prevent early arteriosclerotic lesions (subintimal oedema with splitting of elastica). The early arteriosclerotic lesions appear to be initiated by vascular dissemination of Ni3S2 particles immediately post-injection, whereas the erythrocytosis, amino acid disturbances, and advanced arteriosclerotic lesions depend upon continued presence of the Ni3S2-injected kidney. Resection of the contralateral (non-injected) kidney has no effect upon Ni3S2-induced erythrocytosis, arteriosclerosis, or amino acid disturbances. Glomerulomegaly and mesangial hyperplasia developed in control rats following unilateral nephrectomy, owing to compensatory renal hypertrophy. Glomerulomegaly was more pronounced in Ni3S2-treated rats following contralateral nephrectomy than following ipsilateral nephrectomy, suggesting that erythrocytosis and compensatory renal hypertrophy act synergistically to enhance glomerulomegaly.

Animals↗

PubMed1988

Platelets, platelet-derived growth factor and arteriosclerosis.

Platelets participate in the pathogenesis of arteriosclerosis and in the progression of atherosclerosis by adhering to the damaged arteries and subsequently forming mural thrombi which are either swept away and embolize or are endothelialized and thus become part of the vessel wall. Rheologic considerations predict and blood perfusion experiments using flow chambers with exposed vessel wall components demonstrate that platelet participation increases with the wall shear rate and is thus particularly important in stenosed arteries (acute thrombosis) and the microvasculature (hemostasis). In addition to their involvement in thrombosis, activated platelets release growth factors, most notably a platelet-derived growth factor (PDGF) which may be the principal mediator of smooth muscle cell migration from the media into the intima and of smooth muscle cell proliferation in the intima as well as of vasoconstriction. The recent discovery that PDGF can be produced by additional cells involved in the pathogenesis of arteriosclerosis (endothelial cells, monocytes/macrophages, smooth muscle cells themselves) and that they may play a role in tumorigenesis has tremendously increased the interest in this growth factor and in potential antagonists.

Animals↗

PubMed1978

Cholesterol and repair processes in arteriosclerosis.

The high cholesterol content of the atheroma and the correlation between elevation of the serum cholesterol and myocardial infractions gave rise to the lipid theory of arteriosclerosis, which assumes that cholesterol induces arteriosclerotic lesions and that its reduction counteracts their development. However, many facts contradict this theory. Therefore, a new hypothesis has been based on the high cholesterol content of old pathological lesions of granulomatous nature and the similarity of atheromata to granulomas. In the latter, a complicated tissue containing a high percentage of cholesterol is deposited in response to the injurious agent, which becomes walled off by this tissue. Thus, cholesterol forms part of a protective mechanism, a hypothesis compatible with the known facts about the relationship of cholesterol to arteriosclerosis.

Arteriosclerosis↗

PubMed1998

Intrarenal arteriosclerosis and impairment of kidney function in NIDDM subjects.

It is currently under debate whether the pathogenesis of end-stage renal failure in non-insulin-dependent diabetes mellitus (NIDDM) is a consequence of microangiopathy alone. The aim of this study was to investigate intrarenal arteriosclerosis and its correlation with kidney function in NIDDM. In 36 diabetic subjects, and in 10 age- and sex-matched healthy control subjects we measured kidney volume and resistive index of the interlobar arteries by duplex Doppler ultrasonography. Clinical and metabolic parameters, renal function and vascular sequelae of the disease were also evaluated. In diabetic subjects resistive index (median 0.72, range 0.54-0.79) was higher than in control subjects (median 0.62, range 0.57-0.66) (2p < 0.002). Kidney volume and resistive index correlated with age (p < 0.004), body mass index (p < 0.001), mean blood pressure (p < 0.001), total and LDL cholesterol (p < 0.01) and creatinine clearance (p < 0.001 and < 0.01, respectively). Kidney volume also correlated with HbA1 (p < 0.01) and resistive index with uric acid (p < 0.01). Lower body macroangiopathy was associated with increased resistive index and reduced kidney volume (2p < 0.05), while upper body macroangiopathy and microangiopathy were not. Our data suggest that macroangiopathy rather than microangiopathy is mainly responsible for impairment of kidney function in NIDDM. The resistive index of interlobar arteries seems to be a reliable marker of intrarenal arteriosclerosis and can be used as a non-invasive, easily available parameter of its evolution.

Arteriosclerosis↗

PubMed2001

[Possibilities of regression in arteriosclerosis].

We studied the hypercholesterolemic rabbit model in order to evaluate potentials of regression of arteriosclerosis by measuring various blood and plaque parameters. After induction of arteriosclerosis by feeding a 2% cholesterol-enriched diet (CHF) for 6 weeks, the highly increased blood lipid levels decreased significantly under normal diet, while the cholesterol concentration, the lumen stenosis, and the number of smooth muscle cells in the plaques of the thoracic aorta still significantly increased. Sixty-eight weeks after reaching normal blood lipid levels, cellular density and number of macrophages significantly diminished; cholesterol concentration and lumen stenosis did not change significantly, whereas the smooth muscle cells further increased. Arteriosclerotic arteries of elderly people demonstrated a similar structure as seen after long-term regression in our experiments.

Animals↗

PubMed2001

[Significance of the uPA/uPAR system for development of arteriosclerosis and restenosis].

Arteriosclerosis and the development of restenosis still remain a significant clinical problem. Migration of vascular smooth muscle cells from the media to the intima and cell proliferation are the hallmarks of the underlying pathomechanisms. Cell migration requires chemotaxis, phenotypic changes of cells, cell adhesive and de-adhesive events and the coordinated remodeling of the extracellular matrix. One of the phenotypic changes induced in migrating cells is the increased expression of urokinase plasminogen activator (uPA) and of its specific receptor uPAR. They are polarized to the leading edge of migrating cells. Both uPA and uPAR are key mediators of extracellular proteolysis. They participate in extracellular matrix remodeling, activate cells and enable them to migrate and invade into different tissue layers. UPA/uPAR are multifunctional proteins influencing a great variety of signal transduction pathways ultimately culminating in the regulation of cell migration and proliferation. In addition to time- and space-confined proteolysis this powerful system can mediate chemotaxis, cell adhesion and gene expression, partly by interacting in concert with integrins, G proteins, or with yet unidentified coreceptors or adapter molecules. Interaction with the uPA/uPAR system or components of its specific signal transduction pathways may serve as a guide for the development of effective therapeutic strategies to prevent arteriosclerosis and restenosis after percutaneous arterial angioplastic interventions.

Animals↗

PubMed1995

Effect of oestrogen replacement therapy on development of experimental arteriosclerosis: a study in transplanted and balloon-injured rabbit aortas.

The mechanism underlying possible protection of oestrogen replacement therapy against cardiovascular disease appears to go beyond beneficial changes in plasma lipoproteins. A direct action of oestrogen on the metabolism of lipoproteins after entering the arterial wall may occur. The present study evaluated whether oestrogen replacement therapy affects the development of experimental arteriosclerosis in immunologically injured (experiment A + B) and balloon-injured (experiment B) aortas in ovariectomized rabbits maintained at a human level of plasma cholesterol; both models involve severe damage to the endothelium with resulting rapid accumulation of lipoproteins in the arterial intima and therefore appear suitable for studying factors directly affecting subendothelial lipoprotein metabolism. In experiment A, dietary cholesterol required to maintain a human level of plasma cholesterol was significantly higher for the oestrogen group than for the placebo group. Similarly, cholesterol accumulation in the aortic grafts was borderline higher for the oestrogen than the placebo group, whilst intimal hyperplasia was without difference between the groups. Due to a modified schedule of cholesterol feeding in experiment B, oestrogen and placebo groups received the same amount of dietary cholesterol, and cholesterol accumulation and intimal hyperplasia were similar in immunologically injured and balloon-injured parts of the aorta in both groups. These results suggest that in the female rabbit maintained at a human level of plasma cholesterol, oestrogen replacement therapy has no direct action on the development of experimental arteriosclerosis when induced by immunological or mechanical injury to the endothelium.

Animals↗

PubMed1984

Exercise and risk factors for arteriosclerosis in 42 married couples followed over four years.

Forty-two married couples (30-69 years of age) were followed for 4 years with yearly measurements of risk factors for arteriosclerosis. Advice was given concerning relaxed, enjoyable exercise (mainly running at 10-13 km hr-1). Each person served as his own control by comparison of the first and the last yearly status. Both the group of women and the group of men significantly improved (two sided p less than 0.005) their maximum oxygen uptake, and reduced their blood glucose concentration (two-sided p less than 0.01). S-cholesterol (for the group of men) was reduced statistically significantly (two-sided p less than 0.01). At the first examination the groups of women and men with the lowest maximum oxygen uptake (group I) had higher average values for risk factors than the more active groups (group II). At the final examination almost all persons had improved their maximum oxygen uptake, so none of the other risk factor differences between groups I and II were statistically significant. Both the women and the men improved their well being and their health profile as evaluated in terms of risk factors for arteriosclerosis. Exhaustive exercise was not necessary for beneficial effects.

Adult↗

PubMed1988

Adaptive changes in aging and arteriosclerosis--role of cholesterol.

The "lipid theory" assumes that cholesterol has a causal part in the development of arteriosclerosis; however, in view of the fact that cholesterol has always accompanied life processes, the "lipid theory" contradicts the evolutionary principle of "teleonomy" which predicts that long lasting metabolic effects must have beneficial consequences. Support for the theory was claimed from the correlation between high serum cholesterol and arteriosclerotic complications, from observations in cholesterol fed animals and from cardiac lesions in familial hypercholesterolemia. However, correlations do not prove causality; whether the animal experiments and the observations in familial hypercholesterolemia are pertinent is questionable. Therefore, the possibility was considered that the cholesterol changes are an adaptive mechanism. This is supported by the "normal" cholesterol content of the early lesion, by the stabilization of the DNA helix by cholesterol in appropriate concentration, by the beneficial effects of cholesterol-rich granulomata; by recent reliable "intervention" trials with low cholesterol diets and by the observation that persons dying from ischemic heart disease (having high serum cholesterol) live at least as long as those dying from other causes. Furthermore, studies with serum cholesterol lowering drugs are difficult to interpret and often misleading. The symptomatology of the serum cholesterol changes in arteriosclerosis suggests that they belong to the adaptive aging phenomenon. This would be in line with evolutionary thinking.

Aging↗

PubMed1991

Is arteriosclerosis a life prolonging, adaptive process?

Arteriosclerosis is believed by many to represent the aging process of arteries and to be responsible for the cause-specific deaths at any age in industrialized countries. However, the increasing rate of (A) associated with steadily increasing life expectancy invited studies of the average age at death (AAD) of conditions with prominent (A) (ischemic heart disease, myocardial infarction, cerebrovascular disease, "atherosclerosis"). Data were obtained from "Vital Statistics of the U.S.A.", (Vol. II, Mortality), Section 8, Tables VIII-V). Persons above the age of 40 were studied. The (A) groups were compared to the "normals" from whom (in addition to the groups with prominent arteriosclerosis,) accidents, suicides, homicides and other "external" causes of death were deducted. We also excluded malignancies because the AAD would have prejudiced the data in favor of our assumption. In general the (A) groups had significantly higher (AAD's) than the "normals". Exceptions were white males with ischemic heart disease whose (AAD) was lower than that of the "normals". This was also true for white males and females with myocardial infarction. Although (A) may exceed its normal function leading to lesions (e.g., myocardial infarction) in the majority of the cases it seems to be a life prolonging adaptive process which is in line with evolutionary expectations.

Adaptation, Physiological↗

PubMed1990

Activation of coagulation and fibrinolysis in patients with arteriosclerosis: relation to localization of vessel disease and risk factors.

Activation markers of blood coagulation and fibrinolysis and several fibrinolytic parameters were determined in arteriosclerotic patients to investigate the relation between extension and main localization of vessel disease, risk factors and disturbances within the blood coagulation and the fibrinolytic system. Indications of an increased intravascular fibrin formation and subsequent fibrinolysis were found in peripheral artery disease (PAD) patients but not in coronary artery disease (CAD) patients. Compared with healthy controls PAD patients had elevated TAT (median: 3.2 ng/ml, 1.5-70 vs. 2.1, 1.2-4.7, p less than 0.005) and D-Dimer (median: 365 ng/ml, range 85-2000 vs. 185, 79-360; p less than 0.0001) plasma levels, whereas TAT (2.4, 1.2-13) and D-Dimer (190, 58-1000) levels of CAD patients were in the normal range. No associations were detected between risk factors of arteriosclerosis (hyperlipidemia, diabetes mellitus, cigarette smoking, hypertension) and the plasma levels of the activation markers TAT and D-Dimer. Independent from risk factors PAD and CAD patients had elevated plasma plasminogen activator inhibitor capacity (PAI cap). Our results provide evidence that 1) increased plasma levels of blood coagulation and fibrinolysis activation markers are not related to risk factors of arteriosclerosis but seem to be unspecifically caused by activation processes on arteriosclerotic vessel wall defects, 2) increased plasma PAI cap found in arteriosclerotic patients is a relatively unspecific phenomenon associated with arterial vessel disease.

Antithrombin III↗

PubMed1984

Environmental validation of the homocystine theory of arteriosclerosis.

It has been proposed that elevated concentrations of homocystine in vascular tissue could cause arterial damage leading to arteriosclerosis. This theory is indirectly supported by research in the area of environmental toxicology, which has revealed that carbon monoxide and carbon disulfide, agents whose prolonged exposure is known to result in the development of arteriosclerotic changes, induced vitamin B6 deficiency states which predictably lead to a homocystinuria-like state. Such information provides strong indirect support of the controversial homocystine theory of arteriosclerosis.

Adult↗

PubMed1987

Water and arteriosclerosis.

Consumption of hard water is presumed to protect against the development of arteriosclerotic diseases. Substantial epidemiologic correlations support the "hard water effect" as sufficiently valid to warrant alteration of public water supplies as a public health measure. A recently proposed theory that arteriosclerosis is an indolent, chronic, infectious disease caused by cyanobacteria suggests that an alternate explanation may be possible. The relationship between hard water and arteriosclerosis is reviewed, contradictions and exceptions noted, and an alternate theory of microbial infection is offered.

Arteriosclerosis↗

PubMed2004

Vitamins in human arteriosclerosis with emphasis on vitamin C and vitamin E.

INTRODUCTION: This review focuses on the process of arteriosclerosis arising from oxidative stress on lipoproteins and the general failure of randomized human trials using vitamins to retard this process. REVIEW: As well as clinical trials, the paper reviews the mechanisms by which a variety of oxidants act. Antioxidants are discussed, emphasizing interactions of vitamins C and E with transition metals that can lead to prooxidation. There is a focus on interactions between supplemental or co-antioxidants that counterbalance prooxidant effects of one another. CONCLUSIONS: It is concluded that normal cellular supplementation mechanisms are poorly accessible in the arteriosclerotic plaque leading to a prooxidant environment in which the haphazard introduction of vitamins could potentially be hazardous. Continued investigations into basic and clinical redox interactions of the kind discussed in this review using new measuring techniques may lead to approaches whereby antioxidants can be introduced into tissue in controlled ways for reducing arteriosclerosis.

Animals↗

PubMed2005

Adventitial progenitor cells contribute to arteriosclerosis.

Accumulating evidence indicates the involvement of vascular progenitor cells in the development of arteriosclerosis, including transplant arteriosclerosis, angioplasty-induced restenosis, vein graft atherosclerosis, and spontaneous atherosclerosis. Recently, it was found that the adventitia of the arterial wall contains a large number of progenitor cells, which can differentiate into smooth muscle cells in vitro and in vivo. These progenitor cells were able to migrate from the adventitia into the intima, where they accumulate to contribute to atherosclerotic lesions of vein grafts in apoE-deficient mice. Thus, these cells may be a source of smooth muscle cells and might have implications for cellular, genetic, and tissue engineering approaches to vascular disease.

Animals↗

PubMed2006

Experimental study on genistein prevention and treatment of transplant arteriosclerosis in aortic transplants of rat.

OBJECTIVE: Our objective was to study the effects of genistein, a soy isoflavone, on transplant arteriosclerosis, in addition to its immunosuppressive and antioxidant properties. MATERIALS AND METHODS: We performed male Brown-Norway to male Lewis aortic transplantation. The recipients were randomly assigned to 3 groups: no treatment controls, dimethyl sulfoxide (DMSO; 5 mL/kg) solvent controls, and experimental group that received genistein (20 mg/kg/d) by daily intraperitoneal injection. On postoperative day 60, the graft was harvested and blood obtained. The transplanted aorta was analyzed by histology and immunohistochemistry. The serum was analyzed by an enzyme-linked immunosorbent assay (ELISA). RESULTS: Compared with the 2 controls, leukocyte recruitment to the graft was significantly inhibited by genistein, with a profound reduction in the number of CD69 macrophages infiltrating the adventitia of the transplanted aortas. Moreover, genistein significantly inhibited the expression of VEGF and IFN-gamma production (P < .01). CONCLUSION: These results suggested that the protein tyrosine kinase inhibitor genistein inhibited graft arteriosclerosis.

Animals↗

PubMed1998

Mouse model of venous bypass graft arteriosclerosis.

Saphenous vein grafts are widely used for treatment of severe atherosclerosis via aortocoronary bypass surgery, a procedure often complicated by later occlusion of the graft vessel. Because the molecular mechanisms of this process remain largely unknown, quantitative models of venous bypass graft arteriosclerosis in transgenic mice could be useful to study this process at the genetic level. We describe herein a new model of vein grafts in the mouse that allows us to take advantage of transgenic, knockout, or mutant animals. Autologous or isogeneic vessels of the external jugular or vena cava veins were end-to-end grafted into carotid arteries of C57BL/6J mice. Vessel wall thickening was observed as early as 1 week after surgery and progressed to 4-, 10-, 15-, and 18-fold original thickness in grafted veins at age 2, 4, 8, and 16 weeks, respectively. The lumen of grafted veins was significantly narrowed because of neointima hyperplasia. Histological and immunohistochemical analyses revealed three lesion processes: marked loss of smooth muscle cells in vein segments 1 and 2 weeks after grafting, massive infiltration of mononuclear cells (CD11b/18+) in the vessel wall between 2 and 4 weeks, and a significant proliferation of vascular smooth muscle cells (alpha-actin+) to constitute neointimal lesions between 4 and 16 weeks. Similar vein graft lesions were obtained when external jugular veins or vena cava were isografted into carotid arteries of C57BL/6J mice. Moreover, no significant intima hyperplasia in vein-to-vein isografts was found, although there was leukocyte infiltration in the vessel wall. Thus, this model, which reproduces many of the features of human vein graft arteriosclerosis, should prove useful for our understanding of the mechanism of vein graft disease and to evaluate the effects of drugs and gene therapy on vascular diseases.

Anastomosis, Surgical↗